COPD (thing)

Chronic Obstructive Pulmonary Disease (COPD)

COPD is a chronic, slowly progressing disease characterised by a persistant limitation to airflow that varies very little. COPD is used to describe a spectrum of diseases that includes:

Chronic Bronchitis

Emphysema

Chronic Asthma that has stopped responding to treatment

Small Airways Disease.

COPD is classified according to its severity:

Mild COPD

A clinical diagnosis is given where there is a productive cough on most days for three consecutive months in two successive years. This can be labelled Simple Bronchitis, and is characterised by excessive secretion of bronchial mucus with little airflow obstruction (Tortora, 2000).

The single most important cause of COPD is cigarette smoking. Active smoking causes mucus hypersecretion and a decline in lung function (Barnes, 2001). Air pollution, occupational exposure to dust, fumes and solvents, and repeated chest infections have also been implicated.
Inhaled irritants lead to chronic inflammation of the lung lining which stimulates the mucus glands to enlarge and multiply. Therefore more mucus is produced, which serves to narrow the airways and inhibit ciliary function (Tortora, 2000).

Clinical features of mild COPD include a smoker’s cough and mild dyspnoea with no other abnormal signs. Early COPD is detectable only by carrying out a lung function test using a spirometer (Bellamy & Brooker, 2000).

Moderate COPD

Follows the same pathway as mild COPD, and can be called Chronic Bronchitis (Bellamy & Brooker, 2000). It is characterised by excessive secretion of bronchial mucus with some airflow obstruction (Tortora, 2000).

In moderate COPD the cilia are destroyed trapping the mucus, which may become infected therefore preventing oxygen from diffusing into the blood (Halpin, 2001). The infected mucus may attract an immune response, which unfortunately aids in the destruction of the walls of the alveoli.

Clinical features of moderate COPD include a productive cough, thickened sputum, and dyspnoea on exertion with some abnormal signs. Examination of the chest may show it to be slightly hyperinflated i.e. the diameter of the chest is slightly enlarged, and wheezing noises may be heard (Halpin, 2001).

Severe COPD

Again is a progression of mild and moderate COPD, and can be called Emphysema. It is characterised by excessive secretion of mucus, severe airflow obstruction and widespread destruction of the alveolar walls (Barnes, 2001).

Repeated chest infections cause a battleground effect in the alveoli. The leukocytes involved in the immune response die and as the excessive mucus is blocking access to the blood stream they remain in the alveoli. As the leukocytes die they release an enzyme that destroys the alveolar walls producing abnormally large airspaces. These abnormal airspaces remain filled with air during expiration and so reduce the lung capacity. They also have a reduced surface area available for oxygen diffusion (Halpin, 2001).

Clinical features of severe COPD include a productive cough, thickened and purulent sputum, and breathlessness on any activity. Findings upon examination of the patient with severe COPD may include: hyperinflation of the chest (causing it to look barrel shaped), wheezing and peripheral oedema (Halpin, 2001).

Traditionally patients with severe COPD are divided into two categories:

Blue Bloaters – Cannot get enough oxygen into their system (hypoxaemia) and cannot get carbon dioxide out (hypercapnia). This places a strain on their heart and they develop peripheral oedema (Halpin, 2001). The ‘blue’ derives from the cyanosed appearance of these patients, while ‘bloater’ comes from the large body build.

Pink Puffers – suffer from extreme dyspnoea (breathlessness) and so increase their ventilation. This helps them to maintain their normal carbon dioxide and oxygen levels, however it is very exhausting. The ‘pink’ is derived from the reddish appearance of the patient due to the exertion of breathing. While the ‘puffer’ refers to the breathlessness and panting respiration.